Jarasch Nadine, Martin Ulrike, Zell Roland, Wutzler Peter, Henke Andreas
Institute of Virology and Antiviral Therapy, Medical Center, Friedrich Schiller University, Hans-Knöll-Str. 2, 07745 Jena, Germany.
Apoptosis. 2007 Sep;12(9):1633-43. doi: 10.1007/s10495-007-0084-6.
Coxsackievirus B3 (CVB3), together with other enteroviruses of the picornavirus family, is associated with a wide variety of acute and chronic forms of human diseases. Using the murine model of CVB3-caused myocarditis, this pathogen can be detected not only in solid organs but also in different types of immune cells, preferentially in B lymphocytes. Therefore, these cells could represent a non-cardiac virus reservoir and may play an important role with regard to viral dissemination in the infected host. In addition, the infection of specific immune cells might modulate the severity of tissue injury and the pattern of virus-caused pathology in susceptible or resistant individuals. In the present study it could be demonstrated that CVB3 was capable to infect productively a certain percentage of murine CD19(+) B cells. In vivo studies revealed that CVB3 invaded murine CD19(+) B cells during an acute infection. Three days p. i. approximately 0.5-1.0% of these cells were productively infected. This proportion could be decreased up to 45%, if 3 days p. i. mice were intravenously treated with the pan-caspase inhibitors Z-VAD-FMK or Q-VD-OPH. These data were compared with results obtained from CVB3-infected human Raji cells.
柯萨奇病毒B3（CVB3）与微小核糖核酸病毒科的其他肠道病毒一样，与多种急性和慢性人类疾病相关。利用CVB3诱发心肌炎的小鼠模型，不仅可以在实体器官中检测到这种病原体，还能在不同类型的免疫细胞中检测到，尤其是在B淋巴细胞中。因此，这些细胞可能代表了一个非心脏病毒库，并且在病毒在感染宿主中的传播方面可能发挥重要作用。此外，特定免疫细胞的感染可能会调节易感或抗性个体中组织损伤的严重程度以及病毒引起的病理模式。在本研究中，可以证明CVB3能够有效感染一定比例的小鼠CD19(+) B细胞。体内研究表明，在急性感染期间CVB3侵入小鼠CD19(+) B细胞。感染后3天，这些细胞中约0.5 - 1.0%被有效感染。如果在感染后3天给小鼠静脉注射泛半胱天冬酶抑制剂Z-VAD-FMK或Q-VD-OPH，这一比例可降低至45%。这些数据与从CVB3感染的人Raji细胞获得的结果进行了比较。
